Reactivation of Epstein‐Barr virus from latency

@article{Amon2005ReactivationOE,
  title={Reactivation of Epstein‐Barr virus from latency},
  author={Wolfgang Amon and Paul J Farrell},
  journal={Reviews in Medical Virology},
  year={2005},
  volume={15}
}
The general problem in cancer treatment centres on finding agents that specifically affect cancer cells without damaging normal cells. The differences between cancer cells and normal cells are usually very subtle but about 15% of all human cancers involve a virus infection, for example the Epstein‐Barr virus associated cancers. In these cancers, every tumour cell carries the virus in a latent infection but the number of normal cells infected is very low. So a treatment that could somehow cause… Expand
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References

SHOWING 1-10 OF 66 REFERENCES
Biology and disease associations of Epstein-Barr virus.
  • D. Crawford
  • Biology, Medicine
  • Philosophical transactions of the Royal Society of London. Series B, Biological sciences
  • 2001
TLDR
Recent views on the EBV life cycle and its interlinks with normal B-cell biology are described, and how this interrelationship may be upset and result in EBV-associated disease is discussed. Expand
Gene therapy strategies for treating Epstein-Barr virus-associated lymphomas: comparison of two different Epstein-Barr virus-based vectors.
B cell lymphomas in immunocompromised patients frequently contain the Epstein-Barr virus (EBV) genome (MacMahon et al, 1991), suggesting that gene therapy strategies that target EBV-positive cellsExpand
Demonstration of the Burkitt's lymphoma Epstein-Barr virus phenotype in dividing latently infected memory cells in vivo
TLDR
It is shown that most infected cells in the blood express no detectable latent mRNA or proteins, which suggests that BL may be a tumor of a latently infected memory B cell that is stuck proliferating because it is a tumor and, therefore, constitutively expressing only EBNA1. Expand
Eradication of latent Epstein-Barr virus by hydroxyurea alters the growth-transformed cell phenotype.
TLDR
In vitro studies indicated that low concentrations of the ribonucleotide reductase inhibitor, hydroxyurea, completely eliminated Epstein-Barr virus episomes from latently infected Burkitt's lymphoma cell subsets, providing the first example of chemotherapeutic eradication of a latent herpesvirus from any cell population. Expand
Lytic Induction Therapy for Epstein-Barr Virus-Positive B-Cell Lymphomas
TLDR
The addition of GCV to either gemcitabine- or doxorubicin-containing chemotherapy regimens may enhance the therapeutic efficacy of these drugs for EBV-driven lymphoproliferative disease in patients. Expand
Chemotherapy induces lytic EBV replication and confers ganciclovir susceptibility to EBV-positive epithelial cell tumors.
TLDR
It is demonstrated that a variety of chemotherapeutic agents, including cis-platinum, 5-fluorouracil (5-FU), and taxol, induce the switch from the latent to lytic form of EBV infection in tumor cells, and suggests that GCV enhances the efficacy of conventional chemotherapy for the treatment ofEBV-positive epithelial cell tumors. Expand
Immunohistology of Epstein-Barr virus-associated antigens in B cell disorders from immunocompromised individuals.
TLDR
Proliferating B cell lesions developing in a series of immunosuppressed organ transplant recipients and patients with X-linked lymphoproliferative syndrome were examined for Epstein-Barr virus and cellular gene expression using immunocytochemistry and immunoblotting techniques, and results indicate that all the lesions examined were consistent with a latent, nonproductive type of infection. Expand
A novel form of Epstein-Barr virus latency in normal B cells in vivo
TLDR
It is concluded that the EBV-infected cells in vivo are B cells with a nonactivated phenotype, which represents a novel form of latency in normal B cells. Expand
Immunotherapy for Epstein-Barr virus-associated cancers.
TLDR
The safety and efficacy of adoptively transferred, gene-marked virus-specific cytotoxic T lymphocytes as prophylaxis and treatment of EBV-LPD in recipients of T-cell-depleted allogeneic bone marrow and methods for the generation of antigen-specific lines are studied. Expand
Induction of lytic Epstein-Barr virus (EBV) infection in EBV-associated malignancies using adenovirus vectors in vitro and in vivo.
TLDR
The results suggest that induction of lytic EBV infection in tumors, in combination with GCV, may be an effective strategy for treating EBV-associated malignancies. Expand
...
1
2
3
4
5
...